Time‐dependent effects of insulin on Schwann cell proliferation in the in vitro regenerating adult frog sciatic nerve

Ekström, Per; Edbladh, M.; Edström, Anders

doi:10.1002/jnr.490340603

Cited by 7 publications

(3 citation statements)

References 28 publications

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“…The latter cell types could hence be chiefly responsible for the observed increase in CAMP. In support of this, the nonneuronal cells of the cultured and crush-injured frog nerve show increased protein and DNA synthesis concomitant with the rise in cAMP (2 to 3 days, Ekstrom et al, 1993). On the other hand, adenylyl cyclase has been reported to be axonally transported in peripheral nerves (Bray et al, 1971;Carlsen and Anderson, 1982).…”

Section: Discussionmentioning

confidence: 92%

Increased cyclic AMP in in vitro regenerating frog sciatic nerves inhibits Schwann cell proliferation bur has no effect on axonal outgrowth

Ekström¹

1995

J of Neuroscience Research

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In the present study the role of cAMP for axonal outgrowth and Schwann cell proliferation was studied using the cultured frog sciatic nerve. An intrinsic rise in nerve and ganglionic cAMP could be measured as a response to nerve injury, both in vitro and in vivo. Treatment with 0.1-1.0 microM forskolin, an activator of the cAMP-generating enzyme adenylyl cyclase, increased the cAMP content up to 13-fold, but was yet without effect on axonal outgrowth during an 8-day culturing period. HA-1004, an inhibitor of cAMP-dependent protein kinase, also lacked effect on the regeneration. In contrast, the proliferation of Schwann cells, measured as [3H]thymidine incorporation, was inhibited to about 70% of control by forskolin, whereas HA-1004 stimulated proliferation to approximately 130% of control. The results suggest that cAMP is involved in the injury-induced proliferation of Schwann cells of an adult peripheral nerve but that it lacks a central role in the regeneration of sensory axons of such nerves.

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Section: Discussionmentioning

confidence: 92%

Increased cyclic AMP in in vitro regenerating frog sciatic nerves inhibits Schwann cell proliferation bur has no effect on axonal outgrowth

Ekström¹

1995

J of Neuroscience Research

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“…Insulin has been shown to inhibit injury‐induced regeneration of the adult frog sciatic nerve in vitro . The target cell of this inhibitory effect was the Schwann cells, wherein insulin‐induced inhibition of nerve regeneration as measured by DNA and protein synthesis in cultured nerves (65% of controls) was seen.…”

Section: Introductionmentioning

confidence: 99%

Effect of Insulin‐Induced Hypoglycaemia on the Peripheral Nervous System: Focus on Adaptive Mechanisms, Pathogenesis and Histopathological Changes

Jensen

Mølck

Bøgh

et al. 2014

J Neuroendocrinology

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).Insulin-induced hypoglycaemia (IIH) is a common acute side effect in type 1 and type 2 diabetic patients, especially during intensive insulin therapy. The peripheral nervous system (PNS) depends on glucose as its primary energy source during normoglycaemia and, consequently, it may be particularly susceptible to IIH damage. Possible mechanisms for adaption of the PNS to IIH include increased glucose uptake, utilisation of alternative energy substrates and the use of Schwann cell glycogen as a local glucose reserve. However, these potential adaptive mechanisms become insufficient when the hypoglycaemic state exceeds a certain level of severity and duration, resulting in a sensory-motor neuropathy with associated skeletal muscle atrophy. Large myelinated motor fibres appear to be particularly vulnerable. Thus, although the PNS is not an obligate glucose consumer, as is the brain, it appears to be more prone to IIH than the central nervous system when hypoglycaemia is not severe (blood glucose level ≤ 2 mM), possibly reflecting a preferential protection of the brain during periods of inadequate glucose availability. With a primary focus on evidence from experimental animal studies investigating nondiabetic IIH, the present review discusses the effect of IIH on the PNS with a focus on adaptive mechanisms, pathogenesis and histological changes.

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“…These results are in line with the present study, where addition of exogenous CaM to the nerve cultures inhibited the injuryinduced proliferation. Furthermore, the increasing levels of CaM detected in conditioned medium from day 4 onwards coincide with a rapid increase in the proliferation of non-neuronal cells in the cultured frog nerve (Ekstrom et al, 1993).…”

Section: Discussionmentioning

confidence: 80%

Calmodulin and In Vitro Regenerating Frog Sciatic Nerves: Release and Extracellular Effects

Remgård

Ekström

Wiklund

et al. 1995

Eur J of Neuroscience

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Although calmodulin (CaM) is commonly considered to be an intracellular protein, it has been suggested lately that it is released and exerts functions extracellularly. In the present investigation this was studied in in vitro regenerating adult frog (Rana temporaria) sciatic nerves. Using a multi-compartment incubation chamber, the non-neuronal cells in the outgrowth region of such nerves were radiolabelled with amino acid precursors. Based on immunological criteria, these cells were shown to release CaM. When the nerves were treated with CaM, both the outgrowth of sensory axons and the injury-induced proliferation of non-neuronal cells were partially inhibited. The inhibitory effects occurred even when the incubation medium contained as little as 30 pM CaM. Furthermore, treatment with anti-CaM antibodies resulted in reduced outgrowth, which suggested that during normal conditions extracellular CaM is kept at an optimal concentration. Finally, conditioned medium was found to contain several CaM-binding proteins. The present findings may reflect an earlier unknown function of extracellular CaM in controlling various growth mechanisms in integrated tissues.

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Time‐dependent effects of insulin on Schwann cell proliferation in the in vitro regenerating adult frog sciatic nerve

Cited by 7 publications

References 28 publications

Increased cyclic AMP in in vitro regenerating frog sciatic nerves inhibits Schwann cell proliferation bur has no effect on axonal outgrowth

Increased cyclic AMP in in vitro regenerating frog sciatic nerves inhibits Schwann cell proliferation bur has no effect on axonal outgrowth

Effect of Insulin‐Induced Hypoglycaemia on the Peripheral Nervous System: Focus on Adaptive Mechanisms, Pathogenesis and Histopathological Changes

Calmodulin and In Vitro Regenerating Frog Sciatic Nerves: Release and Extracellular Effects

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